News and views on autism research and other musings. Sometimes uncomfortable but rooted in peer-reviewed scientific research.

Saturday, 29 March 2014

Inflaming inflammation and psychiatry

The systematic review published by Mitchell & Goldstein [1] kinda says it all when it comes to our current view of the topic of inflammation and psychiatry, and in particular inflammation and neuropsychiatric conditions such as autism, schizophrenia and attention deficit hyperactivity disorder (ADHD): "There is preliminary evidence for elevated markers of inflammation in this population".

The Mitchell / Goldstein review very sensibly notes that: "the data are inconsistent" and sound the oft-heard call for "Larger, prospective studies [which] are needed to realize the goal of inflammatory markers informing clinical practice". But, there is not escaping that immune function may be doing so much more than just protecting us for the myriad of beasties which wish to either call us home or make a meal of us or both.

As if to further prove the point, I also chanced on the study by Charity Onore and colleagues [4] who alongside some notable names on the autism research scene looked at the concept of maternal immune activation on the inflammatory status of offspring. The name Charity Onore has (again!) been talked about on this blog and some particularly interesting work looking at adhesion molecules and autism (see here); an area which has since been followed up (see here). The focus on the concept of the maternal immune activation (MIA) model is nothing new when it comes to autism research for example (see here and see here) denoting how elevated inflammatory responses at certain critical times during the nine months that made us may have some important consequences for offspring.

The latest Onore paper details how in a mouse model of MIA (based on the artificial stimulation of mother mice using poly I:C as the immunostimulating agent) "macrophage cytokine production in adult offspring" was the experimental target. Macrophages, also known as the 'big eaters' of the immune system, represent an important part of immune function undertaking some important tasks. Again, they have been mentioned in other blog entries, notably with the initial chatter about GcMAF in connection to autism (see here).

Anyhow, based on the MIA model, Onore et al reported that analysis of adult offspring mice samples ("femurs were collected and bone marrow-derived macrophages were generated") for the presence of various cytokines with or without conditions of stimulation (LPS... see here) produced some interesting results. So for example, "a higher production of CCL3", a chemokine, was recorded. Indeed, elevations in CCL3 otherwise known as MIP-1α, was recorded both with and without stimulation leading authors to conclude: "a general increase in production of this chemokine". Their closing remark on their cumulative results being: "Collectively, these data suggest that MIA can produce lasting changes in macrophage function that are sustained into adulthood". I should add 'in mice' to the end of that sentence too.

ABOUT AUTISM SPECTRUM CONDITIONS

Autism or autism spectrum conditions describe several presentations characterised by core issues with social affect and stereotyped or repetitive actions. Diagnosis is made by observation and analysis of developmental history. These are heterogeneous conditions which can carry various co-morbidities and whilst described as life-long are affected by age and maturation. Autism means different things to different people. To some it means a need for life-long support. To others it is part of the varied tapestry of humanity. To all it means a need to foster a welcoming society with appropriate support and opportunities.